Abstract <p>Skeletal muscles and adipose tissue represent the two largesttissue compartments in the human body by mass and volume. The studyof the influence of lipid metabolism on muscle tissue structureand function is of particular interest. The objective of this workwas to evaluate the effect of an HMG-CoA reductase inhibitor (hypolipidemicdrug atorvastatin) on muscle endurance and the morphological stateof skeletal muscle in dystrophin-deficient mdx mice. During the12-week experiment, mdx mice (<i>n</i> =60) were divided into two groups: Group 1 (control, <i>n</i> = 30) fed a standard diet, andGroup 2 (<i>n</i> = 30) received anHMG-CoA reductase inhibitor with food (20 mg/kg/day). Throughoutthe experiment, mouse body weight was measured, and muscle endurancewas assessed using the Wire Hang test. Histological and immunohistochemicalexamination of the diaphragm and quadriceps femoris (rectus femoris)muscle was performed. It was found that Group 2 animals had a statisticallysignificant increase in body weight compared to the control (<i>p</i> &lt; 0.05). No significant intergroupdifferences in muscle endurance indices were found. In Group 2 animals,histological analysis of the muscle revealed a significant increasein the total number of striated muscle fibers (SMFs) and the proportionof dystrophin-positive fibers, as well as an increased number ofdead SMFs. No significant changes were found in the diaphragm. Theobtained data indicate a complex effect of an HMG-CoA reductaseinhibitor on muscle tissue, which leads to an increase in body weightbut does not improve the functional indices of muscle endurance.It was found that an HMG-CoA reductase inhibitor affects the morphologyof the rectus femoris muscle. Namely, the identified structuralalterations (increase in the number of dead SMFs) in the skeletalmuscle of mdx mice against the background of HMG-CoA reductase inhibitor administrationsuggest the myotoxic effect of the drug, which may further contributeto the progression of muscle tissue dystrophy.</p>